The six embryonically-derived DD motor neurons are born evenly spaced along the AP axis in newly hatched larvae and maintain this spacing into adulthood. We have found that components of a planar cell polarity (PCP)-like pathway that includes
prkl-1/Prickle and
vang-1/Van Gogh are important for properly positioning DD motor neurons in the ventral nerve cord. In
prkl-1, and to a lesser extent,
vang-1 mutants, DD neurons are shifted anteriorly and display distinctive cell spacing defects. These defects can be rescued by
prkl-1 or
vang-1 expression from a pan-neuronal promoter suggesting cell-autonomous roles. DA and DB neurons are also mispositioned in
prkl-1 and
vang-1 mutants. Neuronal positioning defects are present in newly hatched larvae suggesting an embryonic origin for the defect. DD1,3,5 and DD2,4,5, derived from left and right sides of the embryo, undergo cell intercalation during the comma stage to form a single line of DD neurons at the midline.
prkl-1 and
vang-1 mutants display DD intercalation defects that are suggestive of a delay in cell intercalation or improper cell-cell neighbor interactions during intercalation. In order to identify new genes involved in cell intercalation and the proper positioning of motor neurons along the AP axis as well as new insight into PCP-like signaling we are in the process of performing a forward genetic screen for DD neuron spacing defects. PCP signaling is known to play an important role in cell intercalation during neural tube and organ morphogenesis in vertebrates. Our findings show for the first time that a PCP-like pathway involving the core components Prickle and Van Gogh is involved in some aspects of cell intercalation during C. elegans development.